In 2015 we investigated the mechanisms by which activated CD8+ T cells unregulated inhibitor molecules and became dysfunctional. We found that the Treg-suppressed CD8+ T cells unregulated expression of SIRPa, the ligand for CD47, which is upregulated on infected cells. Interestingly, SIRPa appears to be a new marker for exhausted/suppressed CD8+ T cells suggesting that blockade of CD47-SIRPa interactions could lead to reactivation of the effector CD8+ T cells, particlulary if done in conjunction with blockade of the PD-1-PDL-1 axis. A patent protection the IP of our findings on CD47 was filed.